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Academic literature on the topic 'Myocardial ischemia/chemically induced'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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Journal articles on the topic "Myocardial ischemia/chemically induced"

Fu, Liang-Wu, and John C. Longhurst. "Functional role of peripheral opioid receptors in the regulation of cardiac spinal afferent nerve activity during myocardial ischemia." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 1 (2013): H76—H85. http://dx.doi.org/10.1152/ajpheart.00091.2013.

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Thinly myelinated Aδ-fiber and unmyelinated C-fiber cardiac sympathetic (spinal) sensory nerve fibers are activated during myocardial ischemia to transmit the sensation of angina pectoris. Although recent observations showed that myocardial ischemia increases the concentrations of opioid peptides and that the stimulation of peripheral opioid receptors inhibits chemically induced visceral and somatic nociception, the role of opioids in cardiac spinal afferent signaling during myocardial ischemia has not been studied. The present study tested the hypothesis that peripheral opioid receptors modulate cardiac spinal afferent nerve activity during myocardial ischemia by suppressing the responses of cardiac afferent nerve to ischemic mediators like bradykinin and extracellular ATP. The nerve activity of single unit cardiac afferents was recorded from the left sympathetic chain (T2–T5) in anesthetized cats. Forty-three ischemically sensitive afferent nerves (conduction velocity: 0.32–3.90 m/s) with receptive fields in the left and right ventricles were identified. The responses of these afferent nerves to repeat ischemia or ischemic mediators were further studied in the following protocols. First, epicardial administration of naloxone (8 μmol), a nonselective opioid receptor antagonist, enhanced the responses of eight cardiac afferent nerves to recurrent myocardial ischemia by 62%, whereas epicardial application of vehicle (PBS) did not alter the responses of seven other cardiac afferent nerves to ischemia. Second, naloxone applied to the epicardial surface facilitated the responses of seven cardiac afferent nerves to epicardial ATP by 76%. Third, administration of naloxone enhanced the responses of seven other afferent nerves to bradykinin by 85%. In contrast, in the absence of naloxone, cardiac afferent nerves consistently responded to repeated application of ATP ( n = 7) or bradykinin ( n = 7). These data suggest that peripheral opioid peptides suppress the responses of cardiac sympathetic afferent nerves to myocardial ischemia and ischemic mediators like ATP and bradykinin.

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Miura, Tetsuji, Takayuki Miki, and Toshiyuki Yano. "Role of the gap junction in ischemic preconditioning in the heart." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 4 (2010): H1115—H1125. http://dx.doi.org/10.1152/ajpheart.00879.2009.

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The gap junction plays roles not only in electrical coupling of cardiomyocytes but also in intercellular transport of biologically active substances. Furthermore, the gap junction participates in decision making on cell survival versus cell death in various types of cells, and a part of reperfusion injury in the heart has been indicated to be gap junction mediated. The contribution of gap junction communication (GJC) and/or mitochondrial “hemichannels” to protective signaling during the trigger phase of ischemic preconditioning (IPC) is suggested by observations that IPC failed to protect the heart when GJC was blocked during IPC. Although ischemia suppresses both electrical and chemical GJC, chemical GJC persists for a considerable time after electrical GJC is lost. IPC facilitates the ischemia-induced suppression of chemical GJC, whereas IPC delays the reduction of electrical GJC after ischemia. The inhibition of GJC during sustained ischemia and reperfusion by GJC blockers mimics the effect of IPC on myocardial necrosis. IPC induces distinct effects on the interaction of connexin-43 with protein kinases, and the phosphorylation of connexin-43 at Ser368 by PKCε is a primary mechanism of inhibition of chemical GJC by IPC. Several lines of evidence support the notion that the modulation of GJC is a part of the mechanism of IPC-induced protection against myocardial necrosis and arrhythmias, though what percentage of IPC protection is attributable to the inhibition of GJC during ischemia-reperfusion still remains unclear.

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Xie, Mengwei, Chunlan Hu, Delin Li, and Shifeng Li. "MicroRNA-377 Alleviates Myocardial Injury Induced by Hypoxia/Reoxygenation via Downregulating LILRB2 Expression." Dose-Response 18, no. 2 (2020): 155932582093612. http://dx.doi.org/10.1177/1559325820936124.

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Background: miR-377 is closely related to myocardial regeneration. miR-377-adjusted mesenchymal stem cells abducted ischemic cardiac angiogenesis. Nevertheless, there were rarely reports about the impact of miR-377 on myocardial ischemia injury. The purpose of this work is that whether miR-377 can protect against myocardial injury caused by hypoxia/reoxygenation (H/R). Methods: Gene expression omnibus database ( http://www.ncbi.nlm.nih.gov/geo/ ; no. GSE53211) was utilized to study the differential expression of miR-377 in patients with an acute ST-segment elevation myocardial infarction and healthy controls. The luciferase activity was determined utilizing the dual-luciferase reporter system. Quantitative real-time polymerase chain reaction and Western blotting were used to measure the messenger RNA and protein level. Results: Low expression of miR-377 and high expression of leukocyte immunoglobulin-like receptor B2 (LILRB2) were identified in patients with myocardial infarction from analyzing the Gene Expression Omnibus data set. Besides, miR-377 expression was downregulated in cardiomyocyte exposed to H/R. Additionally, overexpression of miR-377 could visibly improve cardiomyocyte injury by regulating cell activity and apoptosis. Conclusions: In short, our findings suggested that miR-377/LILRB2 might regard as a hopeful therapeutic target for myocardial ischemic.

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Rodríguez-Sinovas, Antonio, David García-Dorado, Marisol Ruiz-Meana, and Jordi Soler-Soler. "Protective effect of gap junction uncouplers given during hypoxia against reoxygenation injury in isolated rat hearts." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 2 (2006): H648—H656. http://dx.doi.org/10.1152/ajpheart.00439.2005.

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It has been shown that cell-to-cell chemical coupling may persist during severe myocardial hypoxia or ischemia. We aimed to analyze the effects of different, chemically unrelated gap junction uncouplers on the progression of ischemic injury in hypoxic myocardium. First, we analyzed the effects of heptanol, 18α-glycyrrhetinic acid, and palmitoleic acid on intracellular Ca2+ concentration during simulated hypoxia (2 mM NaCN) in isolated cardiomyocytes. Next, we analyzed their effects on developed and diastolic tension and electrical impedance in 47 isolated rat hearts submitted to 40 min of hypoxia and reoxygenation. All treatments were applied only during the hypoxic period. Cell injury was determined by lactate dehydrogenase (LDH) release. Heptanol, but not 18α-glycyrrhetinic acid nor palmitoleic acid, attenuated the increase in cytosolic Ca2+ concentration induced by simulated ischemia in cardiomyocytes and delayed rigor development (rigor onset at 7.31 ± 0.71 min in controls vs. 14.76 ± 1.44 in heptanol-treated hearts, P < 0.001) and the onset of the marked changes in electrical impedance (tissue resistivity: 4.02 ± 0.29 vs. 7.75 ± 1.84 min, P = 0.016) in hypoxic rat hearts. LDH release from hypoxic hearts was minimal and was not significantly modified by drugs. However, all gap junction uncouplers, given during hypoxia, attenuated LDH release during subsequent reoxygenation. Dose-response analysis showed that increasing heptanol concentration beyond the level associated with maximal effects on cell coupling resulted in further protection against hypoxic injury. In conclusion, gap junction uncoupling during hypoxia has a protective effect on cell death occurring upon subsequent reoxygenation, and heptanol has, in addition, a marked protective effect independent of its uncoupling actions.

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Ding, XiaoHui, Fang Hua, Kristopher Sutherly, Jeffrey L. Ardell, and Carole A. Williams. "C2 spinal cord stimulation induces dynorphin release from rat T4 spinal cord: potential modulation of myocardial ischemia-sensitive neurons." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 295, no. 5 (2008): R1519—R1528. http://dx.doi.org/10.1152/ajpregu.00899.2007.

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During myocardial ischemia, the cranial cervical spinal cord (C1–C2) modulates the central processing of the cardiac nociceptive signal. This study was done to determine 1) whether C2 SCS-induced release of an analgesic neuropeptide in the dorsal horn of the thoracic (T4) spinal cord; 2) if one of the sources of this analgesic peptide was cervical propriospinal neurons, and 3) if chemical inactivation of C2 neurons altered local T4 substance P (SP) release during concurrent C2 SCS and cardiac ischemia. Ischemia was induced by intermittent occlusion of the left anterior descending coronary artery (CoAO) in urethane-anesthetized Sprague-Dawley rats. Release of dynorphin A (1-13), (DYN) and SP was determined using antibody-coated microprobes inserted into T4. SCS alone induced DYN release from laminae I–V in T4, and this release was maintained during CoAO. C2 injection of the excitotoxin, ibotenic acid, prior to SCS, inhibited T4 DYN release during SCS and ischemia; it also reversed the inhibition of SP release from T4 dorsal laminae during C2 SCS and CoAO. Injection of the κ-opioid antagonist, nor-binaltorphimine, into T4 also allowed an increased SP release during SCS and CoAO. CoAO increased the number of Fos-positive neurons in T4 dorsal horns but not in the intermediolateral columns (IML), while SCS (either alone or during CoAO) minimized this dorsal horn response to CoAO alone, while inducing T4 IML neuronal recruitment. These results suggest that activation of cervical propriospinal pathways induces DYN release in the thoracic spinal cord, thereby modulating nociceptive signals from the ischemic heart.

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Tang, Zhaobin, Lei Yang, and Xuesong Zhang. "Vitexin mitigates myocardial ischemia reperfusion-induced damage by inhibiting excessive autophagy to suppress apoptosisviathe PI3K/Akt/mTOR signaling cascade." RSC Advances 7, no. 89 (2017): 56406–16. http://dx.doi.org/10.1039/c7ra12151b.

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Li, Fang, Xiao-Xue Fan, Chun Chu, Yu Zhang, Jun-Ping Kou, and Bo-Yang Yu. "A Strategy for Optimizing the Combination of Active Components Based on Chinese Medicinal Formula Sheng-Mai-San for Myocardial Ischemia." Cellular Physiology and Biochemistry 45, no. 4 (2018): 1455–71. http://dx.doi.org/10.1159/000487572.

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Background/Aims: Traditional Chinese medicine (TCM) has been used in clinical practice for thousands of years and has accumulated considerable knowledge concerning the in vivo efficacy of targeting complicated diseases. TCM formulae are a mixture of hundreds of chemical components with multiple potential targets, essentially acting as a combination therapy of multi-component drugs. However, the obscure substances and the unclear molecular mechanisms are obstacles to their further development and internationalization. Therefore, it is necessary to develop new modern drugs based on the combination of effective components in TCM with exact clinical efficacy. In present study, we aimed to detect optimal ratio of the combination of effective components based on Sheng-Mai-San for myocardial ischemia. Methods: On the basis of preliminary studies and references of relevant literature about Sheng-Mai-San for myocardial ischemia, we chose three representative components (ginsenoside Rb1 (G), ruscogenin (R) and schisandrin (S)) for the optimization design studies. First, the proper proportion of the combination was explored in different myocardial ischemia mice induced by isoproterenol and pituitrin based on orthogonal design. Then, the different proportion combinations were further optimized through uniform design in a multi-model and multi-index mode. Finally, the protective effect of combination was verified in three models of myocardial ischemia injured by ischemia/reperfusion, chronic intermittent hypoxia and acute infarction. Results: The optimized combination GRS (G: 6 mg/kg, R: 0.75 mg/kg, S: 6 mg/kg) obtained by experimental screening exhibited a significant protective effect on myocardial ischemia injury, as evidenced by decreased myocardium infarct size, ameliorated histological features, decreased myocardial myeloperoxidase (MPO) and malondiadehyde (MDA), calcium overload, and decreased serum lactate dehydrogenase (LDH), creatine kinase MB isoenzyme (CK-MB), cardiac troponin I (cTn-I) activity. In addition, the interactions of three components in combination GRS were also investigated. The combination, compared to G, R and S, could significantly reduce the concentration of serum CK-MB and cTn-I, and decrease myocardial infarct size, which demonstrated the advantages of this combination for myocardial ischemia. Conclusion: Our results demonstrated that the optimized combination GRS could exert significant cardioprotection against myocardial ischemia injury with similar effect compared to Sheng Mai preparations, which might provide some pharmacological evidences for further development of new modern Chinese drug for cardiovascular diseases basing on traditional Chinese formula with affirmative therapeutic effect.

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Yang, Jing, Hong-shan Yin, Ya-jing Cao, et al. "Arctigenin Attenuates Ischemia/Reperfusion Induced Ventricular Arrhythmias by Decreasing Oxidative Stress in Rats." Cellular Physiology and Biochemistry 49, no. 2 (2018): 728–42. http://dx.doi.org/10.1159/000493038.

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Background/Aims: Arctigenin (ATG) has been shown to possess anti-inflammatory, immunemodulatory, anti-viral, anti-microbial, anti-carcinogenic, vasodilatory and anti-platelet aggregation properties. However, the protective role of ATG in prevention of arrhythmias induced by myocardial ischemia/reperfusion is unknown. The aim of this study was to investigate the anti-arrhythmia effect of ATG in an ischemia/reperfusion injured rat heart model and explore the related mechanisms. Methods: Rats were randomly exposed to sham operation, myocardial ischemia/ reperfusion (MI/R) alone, ATG+ MI/R, pretreated with ATG in low (12.5 mg/kg/day), medium (50 mg/kg/day) and high dose (200 mg/kg/day), respectively. Ventricular arrhythmias were assessed. The activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and the level of malondialdehyde (MDA) in myocardial tissue were determined by chemical analysis. Results: Compared to MI/R, rats pretreated with ATG in doses of 50 mg/kg/day and 200 mg/kg/day showed significantly reduced incidence and duration of ventricular fibrillation, ventricular tachycardia and ventricular ectopic beat (VEB), and decreased the arrhythmia score during the 30-min ischemia. Incidence and duration of ventricular tachycardia, infarction size and arrhythmia scores in these groups were significantly decreased during the 120-min reperfusion. No ventricular fibrillation occurred during the period of reperfusion. Rats pretreated with ATG in doses of 50 mg/kg/day and 200 mg/kg/ day markedly enhanced the activities of antioxidant enzymes SOD and GSH-Px, reduced the level of MDA. No differences were observed between the group pretreated with a low dose of ATG and the sham group. Administration of ATG significantly increased the expression of antioxidant stress protein Nrf2, Trx1 and Nox1. Conclusion: Our data suggested that ATG plays anti-arrhythmia role in ischemia/reperfusion injury, which is probably associated with attenuating oxidative stress by Nrf2 signaling pathway.

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Borschev, Yu Yu, I. Yu Burovenko, A. B. Karaseva, et al. "Modeling of systemic inflammatory response syndrome by chemical induction of colon injury in rats." Medical Immunology (Russia) 22, no. 1 (2020): 87–98. http://dx.doi.org/10.15789/1563-0625-mos-1839.

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Our objective was to develop a model of systemic inflammatory response syndrome (SIRS) by chemical induction of colon injury and antibiotic-associated intestinal dysbiosis in rats with primary visceral obesity (PVO) for studies of myocardial resistance to ischemia-reperfusion injury. The experiments were performed with adult Wistar male rats with PVO under improved conditions of a conventional animal clinic. The chemically induced inflammatory colon disease (CIICD) was accomplished by intragastric administration of a mixture of broad-spectrum antimicrobial agents (AMA) for 3 days. Five days later, immunological and biochemical studies were carried out, as follows: composition of the intestinal microbiota in feces and shortchain fatty acids in blood, morphological changes in the structure of the colon, hemodynamic parameters and myocardial stability with modified Langendorff system. In PVO rats, the mass of visceral fat deposits and the content of lipopolysaccharides (LPS) in the blood were significantly increased when giving them fatcarbohydrate diet (FCD). In animals with CIICD, in addition to LPS, there was a significant increase in proinflammatory cytokine concentration (TNF, IL-8, MCP-1), and after oral administration of the AMA mixture, pronounced disturbances of food behavior and evacuatory function of gastrointestinal tract, deep destructive changes in colon, as well as qualitative and quantitative composition of intestinal microbiota with characteristics typical to the first-grade dysbiosis. High levels were shown for IL-8 cytokine only. An increase in acetic and propionic acid concentrations were shown in blood in animals with CIICD, and, to a greater extent, in rats with antibiotic-induced dysbiosis (AID). FCD was followed by significantly reduced levels of lactobacilli and bifidobacteria in colonic contents. CIICD leads to detection of Escherichia coli, and intestinal dysbiosis leads to the manifestation of Proteus. A comorbid combination of pathological changes in the immune and digestive systems caused a significant increase in the area of myocardial necrosis (by 35 percent) in isolated heart by, thus presuming decreased myocardial resistance to ischemia-reperfusion injury (IRI). The SIRS model induced by chemical trauma to large intestine is aggravated by the introduction of AMAs mixture, and it is characterized by a controlled change in inflammatory markers. Deterioration of morphofunctional characteristics in isolated heart included decrease in resistance to IRI seems to correspond to acute inflammatory bowel disease with induced intestinal dysbiosis. This model can be used in experimental medicine in the field of cardiology, endomicroecology, gastroenterology, and immunology.

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Fisher, Laura. "Retraction: Vitexin mitigates myocardial ischemia reperfusion-induced damage by inhibiting excessive autophagy to suppress apoptosis via the PI3K/Akt/mTOR signaling cascade." RSC Advances 11, no. 8 (2021): 4440. http://dx.doi.org/10.1039/d1ra90024b.

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Retraction of ‘Vitexin mitigates myocardial ischemia reperfusion-induced damage by inhibiting excessive autophagy to suppress apoptosis via the PI3K/Akt/mTOR signaling cascade’ by Zhaobin Tang et al., RSC Adv., 2017, 7, 56406–56416, DOI: 10.1039/C7RA12151B.

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Dissertations / Theses on the topic "Myocardial ischemia/chemically induced"

Thomaz, Petrônio Generoso. "Avaliação de modelo experimental de falência crônica isolada do ventrículo direito." Universidade de São Paulo, 2007. http://www.teses.usp.br/teses/disponiveis/5/5156/tde-11032008-104558/.

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Os modelos experimentais de falência do ventrículo direito (VD) descritos são de difícil execução, por envolverem procedimentos cirúrgicos complexos e dispendiosos, com alta mortalidade e baixa reprodutividade. Também são raros aqueles que promovem falência ventricular exclusiva do ventrículo direito. Com o objetivo de simular a situação clínica de falência ventricular exclusiva do VD, desenvolvemos um modelo experimental de falência crônica isolada do VD, feito através da injeção de etanol intramiocárdico. A disfunção do VD foi induzida em treze cães adultos, através de múltiplas injeções de etanol a 96% (dose total 1ml/kg), na via de entrada e na porção trabecular do VD. Foram analisados parâmetros hemodinâmicos, metabólicos e ecocardiográficos, em condições basais e após indução da falência. Os animais foram mantidos vivos por um período de 14 dias, após o qual foram reoperados e mortos para análise morfológica dos corações. As pressões foram aferidas na artéria femoral, átrio esquerdo (AE), átrio direito (AD), tronco pulmonar (TP) e VD. O fluxo sanguíneo foi medido na aorta e no tronco pulmonar. Na primeira operação, os dados hemodinâmicos foram registrados antes e imediatamente após a indução da falência do VD. Estes parâmetros também foram coletados na reoperação (14 dias pós-indução da falência). Amostras de sangue arterial e venoso foram colhidas simultaneamente ao registro dos parâmetros hemodinâmicos para avaliação dos gases sanguíneos e dosagem de lactato. Foram feitas avaliações ecocardiográficas no pré-operatório, no sexto e no 130 dia pós-operatório (PO). Houve uma mortalidade de 15,4% (2/13). Observou-se uma queda significativa no débito cardíaco pulmonar após a indução da falência e na reoperação (14º PO), quando comparado aos valores medidos no momento basal (p=0,002). Esta queda do desempenho ventricular direito ocasionou um aumento nos valores do lactato venoso, quando comparados os valores basais contra aqueles do pós infusão de etanol (p=0,0001) e com os da reoperação (p=0,0003). Os dados ecocardiográficos revelaram um aumento no volume diastólico do VD, quando comparados os dados basais com aqueles da primeira semana de seguimento (p=0,0001) e com aqueles medidos duas semanas após a indução da falência (p=0,0084). Houve uma queda significativa da fração de ejeção do VD na primeira e segunda semanas em comparação aos valores basais (p=0,0001). A avaliação microscópica feita a partir de amostras retiradas do VD revelou infartos transmurais, com características histológicas compatíveis com infarto de duas semanas de evolução. A injeção de etanol intramiocárdio permitiu a criação de um modelo simples, econômico e reprodutível de falência crônica isolada do VD. A avaliação dos dados hemodinâmicos, ecocardiográficos e bioquímicos medidos nos diferentes momentos do experimento é compatível com a indução de falência grave do VD. Este modelo pode ser útil no estudo da fisiopatologia da falência isolada do VD, bem como na avaliação de assistência ventricular. Isolated chronic right ventricle (RV) dysfunction is difficult to achieve in experimental models, and sometimes very expensive. Some models require complex surgical procedures, with a high mortality rate and low reproducibility. In order to simulate the clinical status of RV failure, we have developed an experimental model of chronic RV failure by injecting local intramyocardial ethanol 96%. A severe RV dysfunction was induced in 13 mongrel dogs by means of multiple intramyocardial injections of ethanol 96% (total dose of 1ml/kg), in the inlet and trabecular portions of the RV. The hemodynamics, metabolic and ecocardiografic parameters were evaluated at baseline condition and after RV failure. The animals were followed for a 14-day period. After that, they were reoperated for pressure measurements, taken from femoral artery, left atrium (LA), right atrium (RA), RV and main pulmonary artery (PA). Blood flow was measured in the aorta (AO) and PA. Metabolic parameters were assessed simultaneously to pressure measurements, with arterial and venous blood samples withdrawn for gas and lactate analysis, and then, they were killed for morphological evaluation of the heart. All the animals were submitted to echocardiographic evaluation before the first operation, on sixth and on de 13th postoperative day. The mortality rate was 15,4% (2/13). There was a significant decrease in the pulmonary blood flow after RV failure induction (p=0,0018), as well as in the reoperation (p=0,002), as compared to baseline. This decrease in RV performance caused an increase in the venous lactate level, when baseline values are compared with pos infarction values (p=0,001) and reoperation (p=0003). The echocardiografic findings revealed an increased RV diastolic volume on the 6th (p=0,0001) and 13th postoperative day (p=0,0084), as compared to baseline values. Conversely, there was a significant decrease in the RV ejection fraction on the 6th and 13th postoperative day, when compared with baseline values (p=0,0001). Microscopic evaluation of RV samples showed transmural infarctions with histological characteristics aged of two weeks. Intra myocardial ethanol injection has allowed the creation of a simple, inexpensive and reproducible model of chronic RV failure. The hemodynamic, metabolic and echocardiographic parameters assessed in different moments of the protocol are compatible with severe RV failure. It may be useful for RV physiology studies of isolated right sided heart failure, as well as in the assessment of ventricular assist devices.

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Ghormley, Michael Roger. "Psychosocial factors in mental stress induced myocardial ischemia /." Digital version accessible at:, 2000. http://wwwlib.umi.com/cr/utexas/main.

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Graeber, Brendon Lewis. "Increase in Peripheral Arterial Tone Predicts Myocardial Ischemia Induced by Mental Stress." Yale University, 2006. http://ymtdl.med.yale.edu/theses/available/etd-06272006-121029/.

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Mental stress ischemia (MSI) is associated with poor prognosis for coronary artery disease (CAD) and is amenable to treatment, yet no easily administered test exists to diagnose it. Given the known increase in systemic vascular tone in response to stress, we studied the ability of peripheral arterial tonometry (PAT), a noninvasive functional measure of arterial tone, to predict those vulnerable to MSI. Seventy-seven patients with chronic stable CAD were subjected to mental stress with concomitant assessment of myocardial perfusion and pulse wave amplitude. Nuclear perfusion imaging was used to document MSI, and PAT was used to measure pulse wave and microarterial tone. A ratio of PAT measurements during stress to those before stress was used to characterize vascular responses. Serum catecholamines and endothelin-1 (ET-1) were simultaneously measured. Subjects who experienced MSI had a lower average PAT ratio than those who did not (0.76 ¡À 0.04 vs. 0.91 ¡À 0.05, P = 0.03). A receiver operating characteristics curve for PAT ratio predicting MSI had an area under the curve of 0.613 (standard error, 0.065, one-sided P = 0.04). Maxima of sensitivity and specificity were observed at a threshold of 0.78 to define an abnormal PAT ratio. Cross-tabulation of groups above and below this threshold with groups of subjects with and without MSI showed a significant predictive relationship between PAT ratio and MSI (P = 0.03). Subjects at or below this threshold (¡Ü0.78) displayed a significant increase in norepinephrine levels during mental stress (235 pg/ml at baseline, 259 pg/ml during mental stress, P = 0.007). Subjects above this threshold (>0.78) displayed a significant decline in their ET-1 levels 24 hours after mental stress (1.15 pg/ml after mental stress, 0.93 pg/ml 24 hours later, P = 0.01), while those at or below threshold had a continued increase. PAT ratio is a complex functional measure of peripheral arterial tone that significantly predicts the occurrence of MSI. It may have clinical value as an easily administered screening test for MSI.

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Hänninen, Helena. "Multichannel magnetocardiography and body surface potential mapping in exercise-induced myocardial ischemia." Helsinki : University of Helsinki, 2002. http://ethesis.helsinki.fi/julkaisut/laa/kliin/vk/hanninen/.

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Bruce, Sharon Diane. "Development of rate related exercise-induced myocardial ischemia and risk of selected coronary diesease endpoints." Thesis, This resource online, 1993. http://scholar.lib.vt.edu/theses/available/etd-11102009-020132/.

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Tejedor, Gascón Sandra. "Development of new advanced therapies to mitigate ischemia-reperfusion-induced injury during acute myocardial infarction." Doctoral thesis, Universitat Politècnica de València, 2023. http://hdl.handle.net/10251/171487.

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[ES] Las intervenciones actuales utilizadas en el ámbito clínico durante el infarto agudo de miocardio (IAM) se centran en la revascularización de la zona isquémica. Entre dichas estrategias, la angioplastia coronaria, procedimiento por el cual se utiliza un catéter para desobstruir la arteria ocluida, es el método más utilizado. Sin embargo, se ha descrito este proceso (conocido como reperfusión) desencadena un daño adicional en el miocardio, por lo que la combinación de dicha intervención con moléculas cardioprotectoras resulta de gran interés para tratar de reducir el tamaño del infarto. El presente trabajo propone dos nuevas moléculas con el fin de precondicionar el área isquémica antes de la reperfusión en el contexto del IAM. La primera estrategia propuesta se ha basado en el aporte de un ácido graso (diDHA) en la zona isquémica antes de la reperfusión para tratar de reducir el estrés de los cardiomiocitos y el número de células muertas antes de la reperfusión. Además, se han sintetizado nanoconjugados basados en la unión covalente de diDHA a un unido covalentemente a un esqueleto polimérico (ácido poli-L-glutámico, PGA) con el fin de incrementar la estabilidad del diDHA y conseguir una liberación controlada de la molécula. Los resultados obtenidos mostraron que la formulación PGA-diDHA6.4 fue la más optimizada, mostrando un mejor efecto en el precondicionamiento de los cardiomiocitos antes de la reperfusión en términos de reducción de apoptosis, generación de especies reactivas de oxígeno y mantenimiento de la función mitocondrial in vitro. Además, dicho nanoconjugado también mostró un modesto efecto terapéutico cuando se administró en modelos in vivo de isquemia-reperfusión en ratas y cerdos, reduciendo el tamaño final de infarto respecto a los grupos control. La segunda estrategia terapéutica propuesta se ha centrado en aumentar el potencial terapéutico de las vesículas celulares de pequeño tamaño (SEV o exosomas) procedentes de medio condicionado de células madre estromales (MSC). Numerosos estudios han descrito el papel terapéutico de factores paracrinos secretados por las MSC, donde se incluyen tanto factores solubles como vesículas extracelulares (EV) y, en especial, SEV. Diversas estrategias, como la modificación genética o precondicionamiento de estas células, han sido utilizadas para aumentar el potencial terapéutico de las mismas. En este trabajo se ha propuesto la modificación genética de las MSC con el objetivo de enriquecer las SEV en proteínas de interés que pudiesen potenciar el efecto terapéutico de las SEV nativas. En base a estudios previos, donde se ha visto que la oncostatina-M (OSM) podría jugar un papel anti-fibrótico en el contexto del IAM, se decidió incorporar dicha proteína en la superficie de las SEV derivadas de MSC mediante su fusión con proteínas presentes de forma natural en la superficie de las SEV, con el objetivo de desencadenar una respuesta en las células diana. La modificación de la secuencia de la OSM y su fusión con la tetraspanina CD81 permitieron cargar de manera efectiva la OSM en la superficie de las SEV, y los resultados preliminares en fibroblastos ventriculares cardíacos mostraron un efecto funcional beneficioso con respecto a los SEV control y los enriquecidos en CD81, reduciendo la tasa de proliferación de las células en condiciones de ayuno, y modificando la expresión y la liberación de la proteína telo-Col1α1 en las células después de ser estimuladas con TGFβ-1, α-dextrano y ácido ascórbico-L-sulfato En resumen, dos nuevas estrategias terapéuticas avanzadas libres de células han sido propuestas en el presente trabajo, donde se han mostrado resultados preliminares prometedores para reducir el daño en el miocardio tras el IAM en términos de reducción de apoptosis de cardiomiocitos y de activación de fibroblastos car [CA] Les intervencions actuals utilitzades en l'àmbit clínic durant l'infart agut de miocardi (IAM) se centren en la revascularització de la zona isquèmica. Entre aquestes estratègies, l'angioplàstia coronària, procediment pel qual s'utilitza un catèter per a desobstruir l'artèria oclosa, és el procés més utilitzat. No obstant això, s'ha descrit que aquest procés (conegut com a reperfusió) desencadena un mal addicional en el miocardi. En conseqüència, la combinació d'aquesta intervenció amb molècules cardioprotectores resulta de gran interés per a tractar de reduir la grandària de l'infart. El present treball proposa dues noves molècules amb potencial cardioprotector en el context del IAM. Com a primera estratègia terapèutica, s'ha proposat l'aportació d'un àcid gras (diDHA) a la zona isquèmica del miocardio abans de la reperfusió per a tractar de reduir l'estrés dels cardiomiocitos i el nombre de cèl·lules mortes abans de la reperfusió. A més, s'han sintetitzat nanoconjugats basats en la unió covalent de diDHA a un esquelet polimèric (àcid poli-L-glutàmic, PGA) amb la finalitat d'incrementar l'estabilitat del diDHA i aconseguir un alliberament controlat de la molècula. Els resultats obtinguts van mostrar que la formulació PGA-diDHA6.4 va ser la més efectiva, mostrant un millor efecte en el precondicionament dels cardiomiocitos abans de la reperfusió en termes de reducció d'apoptosi, generació d'espècies reactives d'oxigen i manteniment de la funció mitocondrial in vitro. A més, el nanoconjugat PGA-diDHA6.4 també va mostrar un modest efecte terapèutic quan es va administrar en models in vivo d'isquèmia-reperfusió en rates i porcs, reduint la grandària final d'infart respecte als grups control. La segona estratègia proposada s'ha centrat en potenciar l'efect terapèutic de vesícules extracelul·lars de xicoteta grandària (SEV o exosomes) que son secretades per cèl·lules mare estromales. Nombrosos estudis han descrit el paper terapèutic de factors paracrinos secretats per les MSC, on s'inclouen tant factors solubles com vesícules extracelul·lars (EV) i, especialment, les SEV. Diverses estratègies, com la modificació genètica o el precondicionament de les MSC, s'han estudiat per augmentar el potencial terapèutic d'aquestes cèl·lules. En aquest treball, es va pensar en la modificació genètica de les MSC amb l'objectiu d'enriquir les SEV en proteïnes d'interés que pogueren potenciar l'efecte terapèutic de les SEV natives. Sobre la base d'estudis previs, on s'ha vist que la oncostatina-M (OSM) podria jugar un paper anti-fibròtic en el context del IAM, es va decidir incorporar aquesta proteïna en la superfície de les SEV derivades de MSC mitjançant la seua fusió amb proteïnes presents de manera natural en la superfície de les SEV, amb l'objectiu de desencadenar una resposta en les cèl·lules diana. La modificació de la seqüència de la OSM i la seua fusió amb la tetraspanina CD81 van permetre carregar de manera efectiva la OSM en la superfície de les SEV, i els resultats preliminars en fibroblastos ventriculars cardíacs van mostrar un efecte funcional respecte als SEV control i els enriquits en CD81, reduint la taxa de proliferació de les cèl·lules en condicions de dejuni, i modificant l'expressió i la secreció de la proteïna telo-Col1α1 en les cèl·lules després de ser estimulades amb TGFβ-1, α-dextran i àcid ascòrbic-L-sulfat, simulant una activació dels fibroblastos in vitro. En resum, dues noves estratègies terapèutiques avançades lliures de cèl·lules han sigut proposades en el present treball, on s'han mostrat resultats preliminars prometedors per a reduir el mal en el miocardi després del IAM en termes de reducció d'apoptosi de cardiomiocitos i d'activació de fibroblastos cardíacs. [EN] Current therapeutic approaches against acute myocardial infarction (AMI) are focused on myocardial ischemic zone revascularization. The most common strategy is called primary angioplasty, in which a catheter is introduced to unblock the affected artery and restore blood flux, in a process called reperfusion. Nevertheless, an additional injury on cardiac tissue is caused after reperfusion, and the combination of primary angioplasty with the use of cardioprotective molecules has emerged as a potential strategy to reduce cardiac tissue injury. Two new cell-free therapeutic strategies to preconditionate myocardial ischemic area before reperfusion have been proposed to reduce cardiac injury after AMI. The first therapeutic strategy proposed consisted on the input of a free fatty acid (di-docosahexaenoic acid, diDHA) covalently bound to a polymeric backbone (poly-L-glutamic acid, PGA) in order to increase diDHA solubility and stability and modulate its effect on target cells. Results showed that PGA-diDHA6.4 conjugate administration during ischemia protected cardiomyocytes from reperfusion-induced injury, as apoptotic number of cells and oxidative stress was reduced, and mitochondrial function was less affected when compared to untreated cells. In addition to this, PGA-diDHA6.4 also showed therapeutic effects when locally administered in an ischemia-reperfusion in vivo model in rats and pigs, where a modest reduction of area at risk was observed compared to control groups. The second cell-free strategy proposed in this work was focused on enhancing the therapeutic potential of small extracellular vesicles (SEV or exosomes) isolated form mesenchymal stromal cells (MSC) conditioned media. Previous studies have described the therapeutic potential of paracrine factors released by MSC, where both soluble factors and vesicular components are included. In particular, SEV have gained special attention. Several stretegies, such as genetic modification or cell preconditioning, have been tested to enhance the MSC therapeutic potential. In this work, it was proposed MSC genetic modification in order to load proteins of interest on SEV and potentiate its native therapeutic potential. Based on previous findings, where it has been described a potential anti-fibrotic role of oncostatin-M (OSM) in AMI context, we decided to incorporate OSM on SEV surface by its fusion to CD81 tetraspanin, a protein naturally loaded on SEV surface, in order to trigger functional effects on target cells. OSM sequence modification was necessary in order to load the protein on SEV surface efficiently, and preliminary data showed that modified OSM-CD81 loaded on SEV had a functional effect on human ventricular cardiac fibroblasts. Concretely, decrease of proliferation rate after starvation and telo-Collagen1α1 location pattern modification was observed after stimulation with a pro-fibrotic cocktail (containing TGFβ-1, α-dextran and ascorbic-L-acid sulphate) in vitro when cells were treated with modified OSM-CD81- SEV compared to ctrl and CD81-loaded SEV treatments. Overall, two new advanced cell-free therapies with preliminary promising results have been proposed in order to reduce myocardial injury after AMI in terms of cardiomyocytes apoptosis reduction and fibrosis mitigation. Tejedor Gascón, S. (2021). Development of new advanced therapies to mitigate ischemia-reperfusion-induced injury during acute myocardial infarction [Tesis doctoral]. Universitat Politècnica de València. https://doi.org/10.4995/Thesis/10251/171487 TESIS

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Fan, Man-hin Michael. "Endotoxin from porphyromonas gingivalis improves recovery of the electrically induced Ca2+ transient following ischemia and reperfusion /." View the Table of Contents & Abstract, 2007. http://sunzi.lib.hku.hk/hkuto/record/B38347945.

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Fan, Man-hin Michael, and 范文軒. "Endotoxin from porphyromonas gingivalis improves recovery of the electrically induced Ca2+ transient following ischemia andreperfusion." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B45011205.

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Oriyanhan, Wnimunk. "Taurine prevents myocardial ischemia/reperfusion-induced oxidative stress and apoptosis in the prolonged hypothermic rat heart preservation." Kyoto University, 2005. http://hdl.handle.net/2433/144379.

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Chin, Reiko. "Effects of Exercise Training on Myocardial Fatty Acid Metabolism in Rats with Depressed Cardiac Function Induced by Transient Ischemia." Kyoto University, 2001. http://hdl.handle.net/2433/150165.

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Books on the topic "Myocardial ischemia/chemically induced"

Michel, Piper Hans, and Preusse C. J, eds. Ischemia-reperfusion in cardiac surgery. Kluwer Academic Publishers, 1993.

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R, Heyndrickx Guy, Vatner S. F, and Wijns William, eds. Stunning, hibernation, and preconditioning: Clinical pathophysiology of myocardial ischemia. Lippincott-Raven Publishers, 1997.

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Guy R., M.D. Heyndrickx (Editor), Stephen F., M.D. Vatner (Editor), and William Wijns (Editor), eds. Stunning, Hibernation, and Preconditioning: Clinical Pathophysiology of Myocardial Ischemia. Lippincott Williams & Wilkins, 1997.

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Thomas, Gregory S., L. Samuel Wann, and Myrvin H. Ellestad, eds. Ellestad's Stress Testing. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190225483.001.0001.

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The 6th edition of the textbook Ellestad’s Stress Testing: Principles and Practice was written for the new and veteran clinician alike performing stress testing. Thoroughly updated, referenced and interspersed with case examples, the book reviews how to get the most out exercise testing, without and with ancillary imaging. In addition to evaluation of ST segment depression, other powerful tools to detect ischemia and forecast the future are reviewed to increase the diagnostic accuracy and prognostic ability of exercise testing. The recognition and significance of exercise induced arrhythmias and conduction defects are examined. When to convert to pharmacologic stress or add ancillary imaging, including myocardial perfusion imaging, echocardiography, coronary calcium scoring, and magnetic reference imaging are reviewed. The use of stress testing in the management of obstructive and non-obstructive coronary artery disease (CAD), heart failure, cardiac rehabilitation, peripheral vascular disease, congenital heart and other cardiovascular diseases (CVD) is examined. Options to optimize the diagnostic capabilities of exercise and other diagnostic testing for women are highlighted. Strategic use of exercise testing in the face of a decreasing burden of CAD in the developed world, as well as the opportunity to rely on exercise testing as the first test to evaluate CVD in the developing world, are reviewed. The fundamentals of exercise physiology and myocardial ischemia that serve as the foundation for exercise testing in health and disease are explained.

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Book chapters on the topic "Myocardial ischemia/chemically induced"

Lavanchy, N., J. Martin, and A. Rossi. "The Role of Beta-Adrenoceptors in Ischemia-Induced Acidosis in the Isolated Rat Heart : A 31-P NMR Study." In Myocardial Ischemia. Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-2055-5_17.

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Vaccarino, Viola. "Mental Stress-Induced Myocardial Ischemia." In Cardiovascular Diseases and Depression. Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-32480-7_8.

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Hoshida, Shiro, Nobushige Yamashita, Kinya Otsu, and Masatsugu Hori. "Antisense-Induced Underexpression of Manganese Superoxide Dismutase Extends Myocardial Ischemia-Reperfusion Injury." In Myocardial Ischemia and Preconditioning. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0355-2_5.

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Zhao, Ting C., and Rakesh C. Kukreja. "Adenosine A3 Receptor induced Delayed Preconditioning: Essential Role of Nuclear Factor κB, Nitric Oxide Synthase and Mitochondrial KATP channels." In Myocardial Ischemia and Preconditioning. Springer US, 2003. http://dx.doi.org/10.1007/978-1-4615-0355-2_23.

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Ferdinandy, Peter, Csaba Csonka, Tamás Csont, Zoltán Szilvássy, and László Dux. "Rapid pacing-induced preconditioning is recaptured by farnesol treatment in hearts of cholesterol-fed rats: Role of polyprenyl derivatives and nitric oxide." In Myocardial Ischemia and Reperfusion. Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-4979-6_4.

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Engler, Robert L., Ughetta del Balzo, and Bruce R. Ito. "Complement-Induced Myocardial Ischemia: Neutrophil and Vascular Mechanisms." In Regulation of Coronary Blood Flow. Springer Japan, 1991. http://dx.doi.org/10.1007/978-4-431-68367-4_24.

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Egstrup, Kenneth. "Combined Treatment of Stable Effort-Induced Angina and Mixed Angina." In Pathophysiology and Rational Pharmacotherapy of Myocardial Ischemia. Steinkopff, 1990. http://dx.doi.org/10.1007/978-3-642-54133-9_17.

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Vegh, Agnes, and James R. Parratt. "Ischemic Preconditioning Markedly Reduces the Severity of Ischemia and Reperfusion-Induced Arrhythmias: Role of Endogenous Myocardial Protective Substances." In Myocardial Preconditioning. Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-662-22206-5_3.

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Guth, Brian D., and Gerd Heusch. "Exercise-Induced Myocardial Ischemia: The Role of Heart Rate Reduction in Therapeutic Approach." In Pathophysiology and Rational Pharmacotherapy of Myocardial Ischemia. Steinkopff, 1990. http://dx.doi.org/10.1007/978-3-642-54133-9_12.

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L’Abbate, A., C. Carpeggiani, M. G. Trivella, I. Simonetti, and A. Biagini. "Myocardial Ischemia Induced by Emotion in Patients with Angina Pectoris." In Developments in Cardiovascular Medicine. Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2587-1_6.

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Conference papers on the topic "Myocardial ischemia/chemically induced"

Mart�nez, Juan Pablo, Olle Pahlm, Michael Ringborn, Stafford Warren, Pablo Laguna, and Leif Sornmo. "The STAFF III Database: ECGs Recorded During Acutely Induced Myocardial Ischemia." In 2017 Computing in Cardiology Conference. Computing in Cardiology, 2017. http://dx.doi.org/10.22489/cinc.2017.266-133.

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Binsch, C., D. Barbosa, K. Jeruschke, et al. "Absence of TBC1D4/AS160 impairs cardiac substrate metabolism and increases ischemia/reperfusion-induced myocardial damage." In Diabetes Kongress 2019 – 54. Jahrestagung der DDG. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1688288.

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Fahmi, Rachid, Brendan L. Eck, Mani Vembar, Hiram G. Bezerra, and David L. Wilson. "Dose reduction assessment in dynamic CT myocardial perfusion imaging in a porcine balloon-induced-ischemia model." In SPIE Medical Imaging, edited by Bruce R. Whiting and Christoph Hoeschen. SPIE, 2014. http://dx.doi.org/10.1117/12.2043748.

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Fahmi, Rachid, Brendan L. Eck, Anas Fares, et al. "Dynamic myocardial perfusion in a porcine balloon-induced ischemia model using a prototype spectral detector CT." In SPIE Medical Imaging, edited by Barjor Gimi and Robert C. Molthen. SPIE, 2015. http://dx.doi.org/10.1117/12.2081547.

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Terres, W., W. Kupper, C. Hamm, and W. Bleifeld. "RESTING MYOCARDIAL ISCHEMIA AFTER INTRAVENOUS INFUSION OF BM 13.177, A THROMBOXANE RECEPTOR ANTAGONIST." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643466.

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We conducted a double blind placebo controlled trial of BM 13.177, a thromboxane receptor antagonist, given intravenously in patients (PTS) with stenoses >70 % of the left anterior descending coronary artery and stable exertional angina pectoris (AP). The study had to be stopped after enrollment of 8 PTS, because 2 had developed resting AP after initiation of the study medication. Both proved to belong to the 4 PTS who had received BM 13.177 (12.5 mg/min). While in one PT, AP was mild, transient and associated with only slight decreases in coronary sinus blood flow (CSBF) and myocardial lactate extraction (MLE), in the other, AP was severe and persisted for 30 minutes in spite of antianginal therapy. Severe clinical symptoms in this PT were associated with a marked fall in MLE from +24 to -121 %. Two PTS under BM 13.177 and 4 on placebo underwent supraventricular stimulation. For both groups, no change in clinical symptoms, CSBF or MLE occured in comparison to a former control stimulation without medication. BM 13.177 led to an inhibition of ex vivo platelet aggregation induced by collagen 1 pg/ml (mean reduction in rate of aggregation by 41 %, p< 0.05), while aggregation was not influenced with collagen 5 μg/ml or ADP. This effect of BM on platelets is explained by its thromboxane receptor blocking properties. The induction of resting myocardial ischemia, however, in 2 of 4 PTS with formerly stable exertional AP may have been the result of either a coronary steal mechanism or an intrinsic stimulation of vascular thromboxane receptors, followed by coronary vasoconstriction.

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NIADA, R., R. Porta, R. Tettamanti, R. Pescador, M. Mantovani, and G. Prino. "DEFIBROTIDE IN EXPERIMENTAL MYOCARDIAL ISCHEMIA IN THE CAT: EFFECTS ON HEMODYNAMICS, ENERGY METABOLISM AND INFARCT SIZE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643152.

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Defibrotide was able to prevent the hemodynamic and biochemical alterations caused by acute myocardial ischemia (AMI) induced by coronary occlusion in the cat when infused 3.5 h before and 5 h after left anterior descending coronary artery (LAD) occlusion. In the platelet perfused heart, Defibrotide was a selective stimulator of coronary vascular PGI^ but not of platelet thromboxane formation. The present study was designed both to investigate the effects of Defibrotide injected 30 min after the induction of acute myocardial ischemia (AMI) in the cat and to evaluate the ability of this drug to reduce infarct size. In the first set of experiments a permanent ligature (5 hours) was placed around LAD. ST segment from ECG, mean aortic pressure (MAP), heart rate (HR) and the pressure-heart rate index (PRI) were considered. Plasma and tissue creatine phosphckinase activity (CFK), tissue lactate and ATP were measured by enzymatic kits from Boehringer Biochemia. 30 min after coronary occlusion a loading dose of Defibrotide (32 ng Kg-1 ) was administered i.v. immediately followed by an infusion (32 ng Kg-1 h 4.5 h-1) MAP, HR and PRI were not modified either by AMI or by the infusion of Defibrotide. AMI-ST segment increases were reduced by Defibrotide from 0.5 h after the beginning of the treatment (—49% vs. AMI control) to the and of experiments (-83% vs. AMI control after 5 h occlusion period). Plasma CFK was reduced from 2.5 h after the beginning of the treatment (-29%) till the end of experiments (-52%). Ischemic tissue CFK, lactate and ATP were normalized by Defibrotide. In the second set of experiments the animals were infused with Defibrotide (50 or 200 mg Kg-1 h-1 , i.v.) starting 2 hours before coronary ligature. The infusion was maintained throughout the 5 h occlusion period. The risk and infarct areas were measured by Evans blu and nitroblue tetrazoliun staining. The 51 ± 3% of risk area was infarcted in AMI control cats. Defibrotide at the two tested doses significantly reduced these infarct areas to 42 ± 4% and 34 ± 2% of risk areas respectively. The beneficial effects of Defibrotide observed in AMI could be attributed both to its ability to enhance PGI2 release from vascular walls and to improved local tissue oxygenation and energy supplies. However it could be taken into account a direct cytoprotective action.

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Walsh, Peter W., Craig S. McLachlan, Leigh Ladd, et al. "Echocardiography Evaluation of a Novel Stable Ovine Heart Failure Model Suitable for Cardiovascular Device Testing." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53824.

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Numerous large animal models of chronic cardiac ischemia have been developed to explore either pathological mechanisms and or device interventions in developed heart failure models. Traditionally chronic heart failure in large animal models such as sheep or pigs has been induced by either coronary ligation with or without reperfusion. Coronary ligation is often attempted in the open chest surgical model or more recently in the closed chest animal via angiography [1]. Both techniques can be challenging and also induce high mortality with the risk of myocardial stunning and resultant shock and or lethal arrhythmias. There is also difficulty in developing stable heart failure across cases where infarct sizes can be variable. One strategy to over come this variability has been via rapid ventricular pacing, however inducing heart failure does not induce sustained heart failure in many cases if the pacing is switched off, and additionally pacing does not induce some of the underlying pathology seen in the development of heart failure [1].

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Wallentin, Lars, Ingyar Nyman, ULF Berglund, and Eva Swahn. "HEPARIN AND ACETYLSALICYLIC ACID (ASA) 75 MG/DAY IN UNSTABLE CORONARY ARTERY DISEASE - EFFECTS ON PLATELET REACTIVITY." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643009.

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In unstable coronary artery disease (UCAD), i.e. unstable angina pectoris (UAP) or non-Q-myocardial infarction (NMI), treatment with heparin or ASA have given encouraging results. The present study attempts to verify the effects of i.v. heparin (5 days) and to evaluate the utility of ASA 75 mg/day (one year). Patients, admitted because of chest pain, who either develops NMI or signs of ischemia in resting or exercise ECG.s are included. Within 72 hours patients are randomized to obtain Heparin+ASA, Heparin+Placebo, Placebo + ASA or Placebo+Placebo . Platelet reactivity is studied in vitro in platelet rich plasma (PRP) in a subgroup of patients.The aggregation response is studied after addition of collagen and ADP and after preincubation with prostacyclin before aggregation with ADP. The figures present results from 85 randomized patients tested before, 5 days, one month and one year after start of therapy.Conclusion: In patients with unstable CAD long term treatment with ASA 75 mg/day inhibits collagen induced platelet aggregation and hampers the ADP response. I.v. heparin tends to raise platelet reactivity and reduce the inhibitory effect of prostacyclin. Heparin induced platelet activation is reduced by simultaneous ASA therapy.

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Saldeen, T., J. Mehta, W. Nichols, and D. Lew. "THROMBOLYSIS BY TISSUE-PLASMNOCEN ACTIVATOR AND A FIBRIN (OCEN) -DEGRADATION PRODUCT, PEPTIDE 6A, IN A CANINE MDDEL OF ELECTRICALLY-INDUCED CORONARY THROMBOSIS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643741.

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Intracoronary thrombus resulting in acute myocardial ischemia can be lysed by thrombolytic agents, such as, streptokinase or t-PA. We examined the potential of a recombitant tissue-plasminogen activator (rt-PA)and a fibrin (ogen)-degradation productpentapeptide 6A, Ala-Arg-Pro-Ala-Lys, corresponding to aminoacids 43-47 in the BB-chain of fibrinogen, which causes marked increase in coronary blood flow and stimulates prostacyclin release, in restoring coronary blood flow in dqgs with experimentally-induced thrombus. An occlusive thrombus was created in the circumflex (Cx) coronary artery in 8 dcgs by electricalstimulation of the endothelial surface. The electrically-induced Cx thrombus consisted primarily of platelets and fibrin. After the occlusive thrcmbus was stable without electrical currant, rt-PA (10ug/kg/minute for 30 minutes intravenously)or peptide 6A (5 unoles/minute for 20 minutes intracorcnary) were randomly administered. Infusion of t-PA restored coronar blood flow (peak 22 ±12 ml/minute, mean ±SD) in five of seven animlas. The time to flow restoration was 12.3 ± 9.1 minutes and the reflow persistedfor20.0 ± 10.9 minutes. Peptide 6A administration also restored coronary blood flow (peak 20 ± 4 ml/ minute) in seven of eight animals with occlusive coronary thrombus. Mean time to blood flow restoration (4.3 ±2.9 minutes) wasshorter(P>0.05) than with rt-PA, but thereflow persisted only for the duration of tine infusion (16.3 ± 10.2 minutes).Peptide 6A adninistration was associatedwith a significant (P±0.05) increase in plasma 6-keto-PGF1α indicating stimulation of prostacyclin release. In addition, plasma t-PA concentrations also increased (F>0.01) at the peak effect of peptide 6A indicating releaseof endogenous t-PA as another potentialmechanism of the thrombolytic effects of peptide 6A. This study demonstrates that peptide 6A exerts coronary thrombolytic effectsccmpa rable to those of t-PA in a canine model of coronary thrombosis.

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Van de Water, A., R. Xhonneux, and F. De Clerck. "ANTI-THROMBOTIC EFFECT IN CANINE CORONARY ARTERIES OF A COMBINED TXA2 synthetase/TXA2-prostaglandin ENDOPEROXIDE RECEPTOR INHIBITOR (R 68070)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643463.

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The effects of R 68070 an oxime-alkane carboxylic acid derivative combining specific thromboxane A2 (TXA2) synthetase inhibition with TXA2/prostaglandin endoperoxide receptor blockade in one molecule, on thrombus formation in a coronary artery following electrically-induced endothelial injury and on its myocardial repercussions were examined in dogs. In an open-chest model in anaesthetized dogs, a stainless steel electrode was inserted into the left anterior descending coronary artery (LAD) distally (+ 1 cm) from an electromagnetic flow probe. ECG and heart rate were derived from limb leads. Serum TXB2 levels were measured by RIA on venous spontaneously coagulated blood (1 h, 37°C). Endothelial cell injury in the LAD coronary artery was induced by the application of an anodal current of 300 μA during 30 min; after an additional 60 min observation period, the thrombus wet weight was determined.In comparison with solvent treatment (n = 8), R 68070 (1.25 mg/kg I.V. 10 min before electrical stimulation, n = 7), significantly reduced the thrombus mass (solvent : 43 mg; R 68070 : 18 mg median value, p < 0.05), the incidence of ECG changes indicative for myocardial ischemia (fibrillation : solvent 1/8; R 68070 0/7; arrhythmias : solvent 3/8; R 68070 2/7; ST changes : solvent 7/8; R 68070 1/7, p < 0.05) and the decrease in coronary blood flow after electrical stimulation (solvent : from 13 to 6.5 ml/min; R 68070 : from 13 to 11 ml/min median values, p < 0.05). Serum TXB2 levels were reduced by 92 % at 100 min after the injection of the active compound (median value, n = 7).Heart rate and coronary blood flow measured before the induction of the endothelial injury were not modified by R 68070.The present study thus demostrates that R 68070 exerts a potent anti-thrombotic effect in canine coronary arteries. The relative contributions to this effect of TXA2 synthetase inhibition and of TXA2/prostaglandin endoperoxide receptor blockade exerted by the compound are being investigated.

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